Hyper-reactive oxygen in the form of superoxide radical is a major cause of intra- and extra-cellular destruction by lipid peroxidation, connective tissue degradation and mutation. Survival of aerobic systems depends upon the inactivation of this radical. The enzyme superoxide dismutase which scavenges these reactive oxygen molecules has been found to be present in ocular tissue. A variety of events leading to ocular damage with impairment of vision may be related to oxygen damage in this manner. Age-related decrease in regulation of intraocular pressure manifested as clinical glaucoma may be caused by destruction mediated by superoxide ions accumulated over the life of an individual. The superoxide level increases in inflammatory processes; an analogous increase in uveitis might predispose to secondary glaucoma. Other anticipated effects related to reactive oxygen might be involved in the formation of cataracts, retinal degenerations and optic nerve damage. This investigation will detail key properties of this enzyme in ocular tissue utilizing experimental animals. Standard models for intraocular inflammation, and for production of experimental glaucoma will be used to document changes in superoxide ion production and inactivation. Some drugs and natural products are known to produce superoxide, in particular flavoproteins and epinephrine. The latter is in common therapeutic use and is implicated in aphakic cystoid macular edema. The role of epinephrine in the production of superoxide will be investigated in this regard.